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. 2019 Feb;9(2):a029249. doi: 10.1101/cshperspect.a029249

Figure 2.

Figure 2.

Glatiramer acetate (GA) treatment modulates type I interferon (IFN) production. GA treatment down-regulates Toll-IL-1 receptor domain–containing adaptor-inducing IFN-β (TRIF) signaling on antigen-presenting cells (APCs), leading to decreased activation of IFN regulatory factor 3 (IRF3) and ATF-2, and subsequent DNA binding of the type I IFN enhanceosome (Molnarfi et al. 2015). Reduction of IFN-β production results in decreased signal transducers and activators of transcription (STAT)1 phosphorylation and activation of proinflammatory cytokines. LPS, Lipid peroxidation; IFNAR, interferon-receptor; TLR, Toll-like receptor; MyD88, myeloid differentiation primary response gene 88; TNF, tumor necrosis factor.